Source:http://linkedlifedata.com/resource/pubmed/id/11964292
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2002-4-19
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pubmed:abstractText |
Resting dendritic cells (DCs) are resident in most tissues and can be activated by environmental stimuli to mature into potent antigen-presenting cells. One important stimulus for DC activation is infection; DCs can be triggered through receptors that recognize microbial components directly or by contact with infection-induced cytokines. We show here that murine DCs undergo phenotypic maturation upon exposure to type I interferons (type I IFNs) in vivo or in vitro. Moreover, DCs either derived from bone marrow cells in vitro or isolated from the spleens of normal animals express IFN-alpha and IFN-beta, suggesting that type I IFNs can act in an autocrine manner to activate DCs. Consistent with this idea, the ability to respond to type I IFN was required for the generation of fully activated DCs from bone marrow precursors, as DCs derived from the bone marrow of mice lacking a functional receptor for type I IFN had reduced expression of costimulatory and adhesion molecules and a diminished ability to stimulate naive T-cell proliferation compared with DCs derived from control bone marrow. Furthermore, the addition of neutralizing anti-IFN-alpha/beta antibody to purified splenic DCs in vitro partially blocked the "spontaneous" activation of these cells, inhibiting the up-regulation of costimulatory molecules, secretion of IFN-gamma, and T-cell stimulatory activity. These results show that DCs both secrete and respond to type I IFN, identifying type I interferons as autocrine DC activators.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
99
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3263-71
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11964292-Animals,
pubmed-meshheading:11964292-Antigen Presentation,
pubmed-meshheading:11964292-Antigens, CD,
pubmed-meshheading:11964292-Autocrine Communication,
pubmed-meshheading:11964292-Bone Marrow Cells,
pubmed-meshheading:11964292-Cell Differentiation,
pubmed-meshheading:11964292-Dendritic Cells,
pubmed-meshheading:11964292-Immunophenotyping,
pubmed-meshheading:11964292-Interferon Type I,
pubmed-meshheading:11964292-Mice,
pubmed-meshheading:11964292-Mice, Inbred C57BL,
pubmed-meshheading:11964292-Mice, Knockout,
pubmed-meshheading:11964292-Mice, Transgenic,
pubmed-meshheading:11964292-Receptors, Interferon,
pubmed-meshheading:11964292-Spleen
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pubmed:year |
2002
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pubmed:articleTitle |
Type I interferons produced by dendritic cells promote their phenotypic and functional activation.
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pubmed:affiliation |
Edward Jenner Institute for Vaccine Research, Compton, Newbury, Berkshire, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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